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Шустерман, Т.Й.; Sela, Shifra; Cohen, Hector; Kristal, Batya; Sbeit, Wisam; Reshef, Ron

doi:10.1023/a:1023741518385

Cited by 27 publications

(3 citation statements)

References 36 publications

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“…MyD88 signal is an important adaptor protein in the process of TLR4 signal transduction, and it is also the upstream signal molecule of the NF-kB signaling pathway, which in turn triggers the signal cascade, resulting in the activation of downstream NF-κB [53]. NF-κB is a marker of intestinal mucosal infection, and the level of NF-κB in colon tissue can reflect the severity of UC disease [54]. Studies have also shown that NF-κB is over-activated in the process of UC, leading to the secretion of pro-inflammatory cytokines, and the accumulation of these inflammatory cytokines is considered to be an important factor in the pathogenesis of colitis [55,56].…”

Section: Discussionmentioning

confidence: 99%

Alleviation Effects of Bifidobacterium animalis subsp. lactis XLTG11 on Dextran Sulfate Sodium-Induced Colitis in Mice

Wang

et al. 2021

Microorganisms

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Inflammatory bowel disease (IBD) is a chronic immune-related disease, which can occur through the dysfunction of the immune system caused by the imbalance of gut microbiota. Previous studies have reported the beneficial effects of Bifidobacterium on colitis, while the related mechanisms behind these effects have not been fully elucidated. The aim of our study is to investigate the alleviation effect of Bifidobacterium animalis subsp. lactis XLTG11 (B. lactis) on dextran sulfate sodium (DSS)-induced colitis and its potential mechanism. The results showed that B. lactis XLTG11 significantly decreased weight loss, disease activity index score, colon shortening, myeloperoxide activity, spleen weight, and colon tissue damage. Additionally, B. lactis XLTG11 significantly decreased the levels of pro-inflammatory cytokines and increased the level of anti-inflammatory cytokine. Meanwhile, high doses of B. lactis XLTG11 significantly up-regulated the expression of tight junction proteins and inhibited activation of Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MYD88)/nuclear factor-κB (NF-κB) signaling pathway. Furthermore, B. lactis XLTG11 increased the gut microbiota diversity and modulated gut microbiota composition caused by DSS. Moreover, Spearman’s correlation analysis also found that several specific gut microbiota were significantly correlated with colitis-related indicators. These results demonstrated that B. lactis XLTG11 can alleviate DSS-induced colitis by inhibiting the activation of the TLR4/MYD88/NF-κB signaling pathway, regulating inflammatory cytokines, improving intestinal barrier function, and modulating the gut microbiota.

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Section: Discussionmentioning

confidence: 99%

Alleviation Effects of Bifidobacterium animalis subsp. lactis XLTG11 on Dextran Sulfate Sodium-Induced Colitis in Mice

Wang

et al. 2021

Microorganisms

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“…Many factors have been implicated in the pathogenesis of UC, such as neutrophil infiltration and overproduction of proinflammatory mediators, including cytokines, arachidonate metabolites, and reactive oxygen metabolites. Proinflammatory cytokines had significantly higher expression and antiinflammatory cytokines had lower expression in the colonic mucosa of UC patients (Ademoglu et al 2004;Danese et al 2004;Shusterman et al 2003;Woodruff et al 2005). Because the increasing lipid peroxidation and mucosal production of reactive oxygen mediators were described in colorectal biopsy specimens of patients with UC, attention has been focused on the role of free radicals in the pathogenesis of UC.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effect and mechanism of proanthocyanidins from grape seeds in rats with TNBS-induced ulcerative colitis

Cai

Qin

et al. 2008

Can. J. Physiol. Pharmacol.

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The aim of the study was to investigate the therapeutic effect and mechanism of proanthocyanidins from grape seeds (GSPE) in the treatment of ulcerative colitis (UC). Rats were intragastrically administered different doses of GSPE (100, 200, and 400 mg/kg) per day for 7 days after UC was twice-induced by intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS)dissolved in 50% ethanol. Sulfasalazine (SASP) at 200 mg/kg was used as a positive control drug. Macroscopic and microscopic damage scores and changes in weight/length ratio (mg/mm) of colon segments were analyzed. The levels of malonyldialdehyde (MDA), interleukin (IL)-1beta, IL-2, IL-4, and myeloperoxidase (MPO) activity in the colon tissues and MPO activity in the serum were all measured by biochemical methods or double antibody sandwich ELISA methods. Compared with the TNBS control group, GSPE treatment facilitated recovery of pathologic changes in the colon after insult with TNBS, as demonstrated by increased body weight (p < 0.01) and decreased colonic weight/length ratio (p < 0.01); GSPE also notably reduced the colonic macroscopic and microscopic damage scores (p < 0.01). The MPO activity in colon tissues and serum of rats treated with GSPE was significantly lower than that in the TNBS control group. The MDA and IL-1beta levels of colon tissues were also decreased in GSPE groups. The intestinal antiinflammatory effect of GSPE was accompanied by a significant improvement of IL-2 and IL-4 levels in the colon tissues of rats in the high-dose GSPE group (p < 0.05). Compared with the SASP group, GSPE groups had no significant difference in the therapeutic effect (p > 0.05). GSPE exerts a beneficial antiinflammatory effect in the acute phase of TNBS-induced colitis in rats by downregulating some of the mediators involved in the intestinal inflammatory response, inhibiting inflammatory cell infiltration and antioxidation damage, promoting damaged tissue repair to improve colonic oxidative stress, decreasing production of proinflammatory cytokines IL-1beta, and increasing production of antiinflammatory cytokines IL-2 and IL-4.

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“…Inflammatory stimuli induce macrophages to secrete TNF-α, which further activates macrophages and nuclear transcription factors such as NF-κB, thereby promoting the release of other inflammatory factors. 21 Apoptosis plays an important role in the late stage of inflammatory reaction, and TLR4/NF-κB is also a key signal to inhibit intestinal epithelial cell apoptosis. 22,23 Studies have shown that TLR4 is involved in the signal pathway of NF-κB nuclear translocation induced by LPS stimulation.…”

Section: Discussionmentioning

confidence: 99%

Carvacrol Ameliorates DSS-Induced Intestinal Inflammation in Rats by Suppressing the TLR4/NF-κB Pathway

Liu

Mao

Zhou

et al. 2022

Natural Product Communications

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The present study aimed to explore the therapeutic effects of carvacrol on the ulcerative colitis (UC) inflammation model induced by DSS (dextran sulfate sodium) in rats. Forty rats were randomly divided into the blank, model, low-, middle-, and high-dose carvacrol groups. The rats drank 4.5% DSS for 5 consecutive days to induce the UC model, except for the blank group. Different concentrations of either carvacrol or purified water were supplied by intragastric administration for 7 consecutive days to assess the protective effect of carvacrol on inflammation in UC rats involving the TLR4/NF-κB signaling pathway. In vivo administration of carvacrol was found to ameliorate the symptoms of colitis in rats. Carvacrol significantly improved the pathological symptoms of colitis in the model group and reduced the DAI and pathological scores of rats. At the same time, carvacrol can reduce the expression of IL-6 and TNF-α induced by DSS, inhibit the activation of TLR4, hinder the nuclear translocation of NF-κB (P65), reduce the cleavage of the apoptosis-related protein cleaved-caspase 3, and protect colon cell apoptosis. The results of in vitro experiments showed that carvacrol has a significant inhibitory effect on cell apoptosis caused by the activation of TLR4 induced by LPS and pcDNA3.1tlr4. Research results revealed that carvacrol has a certain protective effect against inflammation-induced injury in ulcerative colitis rats via inhibiting the activation of the TLR4/NF-κB signaling pathway.

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Cited by 27 publications

References 36 publications

Alleviation Effects of Bifidobacterium animalis subsp. lactis XLTG11 on Dextran Sulfate Sodium-Induced Colitis in Mice

Alleviation Effects of Bifidobacterium animalis subsp. lactis XLTG11 on Dextran Sulfate Sodium-Induced Colitis in Mice

Therapeutic effect and mechanism of proanthocyanidins from grape seeds in rats with TNBS-induced ulcerative colitis

Carvacrol Ameliorates DSS-Induced Intestinal Inflammation in Rats by Suppressing the TLR4/NF-κB Pathway

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